Oxidative Stress in Breeding Bulls: From Redox Biology to Reproductive Performance - A Comprehensive Review

Abstract

Oxidative stress is increasingly invoked to explain subfertility in breeding bulls, yet the term often collapses distinct processes: physiological redox signalling, pathological oxidant excess, and damage induced during semen processing. This critical narrative review integrates evidence across the bull reproductive tract, the ejaculate, cryopreservation, laboratory assessment, and reproductive outcomes. Literature published from 1990 to 29 May 2026 was examined, with earlier foundational studies retained where necessary. The strongest evidence indicates that reactive oxygen and nitrogen species are indispensable at controlled concentrations for capacitation-related signalling, whereas sustained or compartmentally misplaced oxidant production promotes membrane lipid peroxidation, mitochondrial dysfunction, protein modification, impaired acrosomal competence, and sperm DNA damage. Heat load, age-related changes, inflammation, environmental toxicants, and nutritional imbalance can alter the redox environment before ejaculation; centrifugation, oxygen exposure, cooling, freezing and thawing can then amplify injury. Bull-to-bull variation in seminal plasma, sperm membrane composition, antioxidant systems, chromatin packaging and cryotolerance partly explains why conventional motility and morphology assessments fail to identify all subfertile sires. Evidence linking DNA fragmentation and multi-parametric functional phenotypes to field fertility is persuasive but not uniform, because thresholds, assays, semen processing, female factors and fertility definitions differ among studies. Antioxidant supplementation can improve post-thaw traits under selected experimental conditions, but benefits are compound-, dose-, extender- and timing-dependent, and pregnancy or live-birth validation remains uncommon. The field should therefore move from indiscriminate antioxidant addition towards mechanism-informed redox management, longitudinal phenotyping and outcome-linked biomarker panels. A defensible translational model treats oxidative stress not as a single diagnosis but as a dynamic failure of redox regulation across production, processing and fertilisation.